Intelligent Design

Evolution Makes No Sense on This Molecular Clock Problem

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Evolutionary thought did not begin nor end with Charles Darwin. To be sure Darwin was its most important exponent, but evolutionary thinking goes back centuries before 1859 when Darwin first published his book on evolution, and it continued to develop long after Darwin. For example, for all his theorizing Darwin had little idea how biological variation—a crucial, fundamental component of evolutionary theory—actually occurs. How do species change to begin with? About half a century later evolutionists constructed neoDarwinism which added to Darwin’s theory the idea that random genetic mutations provided the needed biological variation which occasionally hit upon improvements which would be preserved via natural selection. Indeed, according to evolution, whales, oak trees, and humans all must have been created by an incredibly long series of random mutations. The theory did not work very well for a number of reasons. For example, mutations don’t slowly add up to arrive at complex biological structures and mechanisms, and biological change is rapid and directed, not slow and random. Those are merely two of a great many false predictions generated by evolutionary theory. One of them is the concept of a molecular clock.  Read more

59 Replies to “Evolution Makes No Sense on This Molecular Clock Problem

  1. 1
    bornagain77 says:

    Dr. Hunter, speaking of evolution making no sense, did you see this article that just came out?

    Newfound groups of bacteria are mixing up the tree of life – June, 15, 2015
    Excerpt: University of California, Berkeley, scientists have identified more than 35 new groups of bacteria,
    The new groups make up more than 15 percent of all known groups or phyla of bacteria, the scientists say, and include the smallest life forms on Earth, microbes a mere 400 nanometers across. The number of new bacterial phyla is equal to all the known animal phyla on Earth.,,,
    the accepted tree of life – a division into the three domains of eukaryotes, which includes animals and plants, bacteria and Archaea – needs to be revised.,,,
    About half of all the genes in these 35-plus phyla are new and unlike other known genes. The recognizable genes suggest that most of the bacteria use a simple process of fermentation to make the energy they need, instead of using aerobic or anaerobic respiration like many other bacteria. They also have unusual ribosomes, the multi-protein machines that translate genetic instructions into proteins. In fact, routine genomic scans would not detect them because of their distinctive 16S ribosomal RNA genes.,,,
    http://phys.org/news/2015-06-n.....-life.html

    In my personal opinion, ‘Now that’s got to hurt’,

    Now That’s Got To Hurt – video
    https://youtu.be/JAkaxQCe51M?t=10

    But I would like to hear your take on it Dr. Hunter. Exactly how did they determine they are not merely new species of bacteria but are a fourth domain of life, and that there are, of all things, 35 new phyla within that new domain of life?

  2. 2
    Zachriel says:

    Cornelius Hunter: Those are merely two of a great many false predictions generated by evolutionary theory.

    The original discovery of the molecular clock was phenomenological, not theoretical. Furthermore, the original observation was that the rate was only approximately constant.

    There are many known factors that can affect the rate of molecular evolution, including generation time, population size, and, of course, natural selection.

  3. 3
    Virgil Cain says:

    How can natural selection affect the rate of molecular evolution?

  4. 4
    Virgil Cain says:

    Those are merely two of a great many false predictions generated by evolutionary theory.

    What evolutionary theory?

  5. 5
    bornagain77 says:

    Zachriel, I have a few questions about random mutations as they pertain to neo-Darwinism. First, since neo-Darwinism is dependent on a fairly large percentage of random mutations being beneficial, in the sense of building up functional complexity, why is it that the vast majority of supposedly beneficial mutations are found to be detrimental in terms of building up functional complexity?

    “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain – Michael Behe – December 2010
    Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain.
    http://behe.uncommondescent.co.....evolution/

    “The neo-Darwinians would like us to believe that large evolutionary changes can result from a series of small events if there are enough of them. But if these events all lose information they can’t be the steps in the kind of evolution the neo-Darwin theory is supposed to explain, no matter how many mutations there are. Whoever thinks macroevolution can be made by mutations that lose information is like the merchant who lost a little money on every sale but thought he could make it up on volume.”
    Lee Spetner (Ph.D. Physics – MIT – Not By Chance)

    Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 – May 2013
    Excerpt: It is almost universally acknowledged that beneficial mutations are rare compared to deleterious mutations [1–10].,, It appears that beneficial mutations may be too rare to actually allow the accurate measurement of how rare they are [11].
    1. Kibota T, Lynch M (1996) Estimate of the genomic mutation rate deleterious to overall fitness in E. coli . Nature 381:694–696.
    2. Charlesworth B, Charlesworth D (1998) Some evolutionary consequences of deleterious mutations. Genetica 103: 3–19.
    3. Elena S, et al (1998) Distribution of fitness effects caused by random insertion mutations in Escherichia coli. Genetica 102/103: 349–358.
    4. Gerrish P, Lenski R N (1998) The fate of competing beneficial mutations in an asexual population. Genetica 102/103:127–144.
    5. Crow J (2000) The origins, patterns, and implications of human spontaneous mutation. Nature Reviews 1:40–47.
    6. Bataillon T (2000) Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? Heredity 84:497–501.
    7. Imhof M, Schlotterer C (2001) Fitness effects of advantageous mutations in evolving Escherichia coli populations. Proc Natl Acad Sci USA 98:1113–1117.
    8. Orr H (2003) The distribution of fitness effects among beneficial mutations. Genetics 163: 1519–1526.
    9. Keightley P, Lynch M (2003) Toward a realistic model of mutations affecting fitness. Evolution 57:683–685.
    10. Barrett R, et al (2006) The distribution of beneficial mutation effects under strong selection. Genetics 174:2071–2079.
    11. Bataillon T (2000) Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? Heredity 84:497–501.
    http://www.worldscientific.com.....08728_0006

    Zachriel, the second question that I have in regards to random mutations as they pertain to neo-Darwinism is, why is it that mutations are found to be not truly random as was postulated within Darwinism’s core theoretical framework?

    WHAT SCIENTIFIC IDEA IS READY FOR RETIREMENT? Fully Random Mutations – Kevin Kelly – 2014
    Excerpt: What is commonly called “random mutation” does not in fact occur in a mathematically random pattern. The process of genetic mutation is extremely complex, with multiple pathways, involving more than one system. Current research suggests most spontaneous mutations occur as errors in the repair process for damaged DNA. Neither the damage nor the errors in repair have been shown to be random in where they occur, how they occur, or when they occur. Rather, the idea that mutations are random is simply a widely held assumption by non-specialists and even many teachers of biology. There is no direct evidence for it.
    On the contrary, there’s much evidence that genetic mutation vary in patterns. For instance it is pretty much accepted that mutation rates increase or decrease as stress on the cells increases or decreases. These variable rates of mutation include mutations induced by stress from an organism’s predators and competition, and as well as increased mutations brought on by environmental and epigenetic factors. Mutations have also been shown to have a higher chance of occurring near a place in DNA where mutations have already occurred, creating mutation hotspot clusters—a non-random pattern.
    http://edge.org/response-detail/25264

    James A. Shapiro PhD. Genetics:
    “What I ask others interested in evolution to give up is the notion of random accidental mutation.”
    http://www.huffingtonpost.com/.....11144.html

    Evolution Is Not Random (At Least, Not Totally) – Tanya Lewis, – 02 October 2014
    Excerpt: Evolution is often said to be “blind,” because there’s no outside force guiding natural selection. But changes in genetic material that occur at the molecular level are not entirely random, a new study suggests. These mutations are guided by both the physical properties of the genetic code and the need to preserve the critical function of proteins, the researchers said.,,,
    “So in the end, most mutation is not random, at least for the DNA sequences we analyzed here,”
    http://m.livescience.com/48103.....2_32724136

    New Research Elucidates Directed Mutation Mechanisms – Cornelius Hunter – January 7, 2013
    Excerpt: mutations don’t occur randomly in the genome, but rather in the genes where they can help to address the challenge. But there is more. The gene’s single stranded DNA has certain coils and loops which expose only some of the gene’s nucleotides to mutation. So not only are certain genes targeted for mutation, but certain nucleotides within those genes are targeted in what is referred to as directed mutations.,,,
    These findings contradict evolution’s prediction that mutations are random with respect to need and sometimes just happen to occur in the right place at the right time.,,,
    http://darwins-god.blogspot.co.....ected.html

    etc.. etc..

    Zachriel, the third question that I have in regards to random mutations as they pertain to neo-Darwinism is, since Darwinism is dependent on random mutations to DNA to provide the raw material for evolution to occur, why are there such elaborate, overlapping, repair mechanisms in place that are dead set against allowing random mutations to occur to DNA in the first place?

    The overlapping repair mechanisms for DNA include, (but are not limited to), the following:

    A proofreading system that catches almost all errors
    A mismatch repair system to back up the proofreading system
    Photoreactivation (light repair)
    Removal of methyl or ethyl groups by O6 – methylguanine methyltransferase
    Base excision repair
    Nucleotide excision repair
    Double-strand DNA break repair
    Recombination repair
    Error-prone bypass
    http://www.newgeology.us/presentation32.html

    Quantum Dots Spotlight DNA-Repair Proteins in Motion – March 2010
    Excerpt: “How this system works is an important unanswered question in this field,” he said. “It has to be able to identify very small mistakes in a 3-dimensional morass of gene strands. It’s akin to spotting potholes on every street all over the country and getting them fixed before the next rush hour.” Dr. Bennett Van Houten – of note: A bacterium has about 40 team members on its pothole crew. That allows its entire genome to be scanned for errors in 20 minutes, the typical doubling time.,, These smart machines can apparently also interact with other damage control teams if they cannot fix the problem on the spot.
    http://www.sciencedaily.com/re.....123522.htm

  6. 6
    bornagain77 says:

    The bottom line is that such sophisticated repair mechanisms, (which, by the way, are orders of magnitude more efficient than man-made repair mechanisms), are incompatible with Darwinism in principle.

    The Evolutionary Dynamics of Digital and Nucleotide Codes: A Mutation Protection Perspective – February 2011
    Excerpt: “Unbounded random change of nucleotide codes through the accumulation of irreparable, advantageous, code-expanding, inheritable mutations at the level of individual nucleotides, as proposed by evolutionary theory, requires the mutation protection at the level of the individual nucleotides and at the higher levels of the code to be switched off or at least to dysfunction. Dysfunctioning mutation protection, however, is the origin of cancer and hereditary diseases, which reduce the capacity to live and to reproduce. Our mutation protection perspective of the evolutionary dynamics of digital and nucleotide codes thus reveals the presence of a paradox in evolutionary theory between the necessity and the disadvantage of dysfunctioning mutation protection. This mutation protection paradox, which is closely related with the paradox between evolvability and mutational robustness, needs further investigation.”
    http://www.benthamscience.com/.....OEVOLJ.pdf

    Contradiction in evolutionary theory – video – (The contradiction between extensive DNA repair mechanisms and the necessity of ‘random mutations/errors’ for Darwinian evolution)
    http://www.youtube.com/watch?v=dzh6Ct5cg1o

    The Darwinism contradiction of repair systems
    Excerpt: The bottom line is that repair mechanisms are incompatible with Darwinism in principle. Since sophisticated repair mechanisms do exist in the cell after all, then the thing to discard in the dilemma to avoid the contradiction necessarily is the Darwinist dogma.
    http://www.uncommondescent.com.....r-systems/

    supplemental question Zachriel. Why is it the random mutation rate is far higher than what even leading Darwinian theorists agree is acceptable for Darwinism to be viable as a theory?

    “it would in the end be far easier and more sensible to manufacture a complete man de novo, out of appropriately chosen raw materials, than to try to fashion into human form those pitiful relics which remained…
    it is evident that the natural rate of mutation of man is so high, and his natural rate of reproduction so low, that not a great deal of margin is left for selection…
    it becomes perfectly evident that the present number of children per couple cannot be great enough to allow selection to keep pace with a mutation rate of 0.1..if, to make matters worse, u should be anything like as high as 0.5…, our present reproductive practices would be utterly out of line with human requirements.”
    Hermann Muller quoted by John Sanford; Appendix 1, Genetic Entropy

    No Matter What Type Of Selection, Mutations Deteriorate Genetic Information – article and animation
    Excerpt: The animation asserts that if harmful mutation rates are high enough, then there exists no form or mechanism of selection which can arrest genetic deterioration. Even if the harmful mutations do not reach population fixation, they can still damage the collective genome.,,,
    Nobel Prize winner HJ Muller (of Muller’s ratchet fame) suggested that the human race can’t even cope with a harmful rate of 0.1 (mutations) per new born. The actual rate has been speculated to be on the order of 100-300 (to as low as 30).
    The animation uses a conservative harmful rate of 1 and argues (with some attempts at humor) that deterioration would thus be inevitable even with a harmful rate of 1 per new born.
    http://www.uncommondescent.com.....ns-weasel/

    Human evolution or extinction – discussion on acceptable mutation rate per generation (with clips from Dr. John Sanford) – video
    http://www.youtube.com/watch?v=aC_NyFZG7pM

  7. 7
    Zachriel says:

    Virgil Cain: How can natural selection affect the rate of molecular evolution?

    Fixation is much faster under selection. The fact that the rate of molecular change is more or less constant is evidence that much of molecular evolution is due to drift, not selection.

    Virgil Cain: What evolutionary theory?

    Here’s an introductory explanation.
    http://evolution.berkeley.edu/.....cle/evo_02

  8. 8
    Virgil Cain says:

    Zachriel:

    Fixation is much faster under selection.

    If the selection pressure stays the same, which we know it doesn’t.

    Here’s an introductory explanation.

    No theory there. Try again.

  9. 9
    bornagain77 says:

    as to:

    “Fixation is much faster under selection.”

    Actually the types of mutations that are most easily fixed under selection (i.e. detrimental) are not the types of mutations that Darwinism needs in order to be viable as a theory:

    Biological Information – Loss-of-Function Mutations by Paul Giem 2015 – video playlist
    (Behe – Loss of function mutations are far more likely to fix in a population than gain of function mutations)
    https://www.youtube.com/watch?v=hzD3hhvepK8&index=20&list=PLHDSWJBW3DNUUhiC9VwPnhl-ymuObyTWJ

    Biological Information – Mutation Count & Synergistic Epistasis (mutation accumulation) 1-17-2015 by Paul Giem – video
    https://www.youtube.com/watch?v=6gdoZk_NbmU

  10. 10
    Virgil Cain says:

    boarnagain77- There was a fruit fly experiment in which no new allele became fixed after over 600 generations- They said:

    We conclude that, at least for life history characters such as development time, unconditionally advantageous alleles rarely arise, are associated with small net fitness gains or cannot fix because selection coefficients change over time.

  11. 11
    Mung says:

    In other words, making measurements based on evolutionary theory leads to problems. The resulting DNA mutation rates are not even close to what we can measure more directly, free from theoretical assumptions.

    Well then, the facts must just be wrong.

  12. 12
    Zachriel says:

    bornagain77: First, since neo-Darwinism is dependent on a fairly large percentage of random mutations being beneficial, in the sense of building up functional complexity,

    False premise. neodarwinism is consistent with most mutations being neutral. Of those mutations that are not neutral, neodarwinism is consistent with most mutations being deleterious.

    bornagain77: why is it that the vast majority of supposedly beneficial mutations are found to be detrimental in terms of building up functional complexity?

    Because most functional complexes are already at local optimums, so any change is likely to be detrimental.

    bornagain77: Zachriel, the second question that I have in regards to random mutations as they pertain to neo-Darwinism is, why is it that mutations are found to be not truly random as was postulated within Darwinism’s core theoretical framework?

    What is the difference between random and “truly random”? In any case, Darwin was at least somewhat Lamarckian in his views of heredity. Modern genetics has found that most mutations are random with respect to fitness, but that the rate of mutation can vary over time and within a genome.

    bornagain77: Zachriel, the third question that I have in regards to random mutations as they pertain to neo-Darwinism is, since Darwinism is dependent on random mutations to DNA to provide the raw material for evolution to occur, why are there such elaborate, overlapping, repair mechanisms in place that are dead set against allowing random mutations to occur to DNA in the first place?

    Those organisms that are more able to accurately replicate themselves, while fending off genomic invaders, are those that persist in the population. However, there’s a tradeoff between accurate reproduction and evolutionary flexibility.

  13. 13
    bornagain77 says:

    With all that hand waving that you do Zach you must be staying very cool this summer. 🙂

    1. Since Darwinism is a non-falsifiable pseudo-science, Darwinism is consistent with anything and everything that may be found. Darwinists merely concoct another epicyclic just so story to cover up embarrassing empirical falsifications. (See Hunter’s false predictions linked in the OP).

    2. Darwinism does not predict ‘local optimums’. In fact supposed Bad Designs, that are supposedly not optimum, (based on the ignorance of Darwinists I might add), have been a staple of Darwinism’s theological core argument against design since day one.

    3. The trade offs, no matter how they are modeled, don’t work:

    Neo-Darwinism’s Catch-22: Before Evolving New Features, Organisms Would Be Swamped by Genetic Junk – Casey Luskin – April 10, 2015
    Excerpt: A new peer-reviewed paper in the journal Complexity presents a computational model of evolution which shows that evolving new biological structures may be deterred by an unavoidable catch-22 problem.,,,
    This is a bit complex — let’s go over it again. Darwinian evolution either (1) produces nothing new, or (2) it’s destined to produce boatloads of deadly junk. In the case of (2), the reward for trying new things is high compared to the cost of building new structures. But in order for the ratio to be high enough for complexity to increase, the cost of building new things must be negligible. Novelties proliferate, but the fraction,, that’s vestigial grows, and the organism is eventually swamped and overwhelmed by harmful vestigial features. However, if you try to avoid the problem of (2) by making the reward-to-cost ratio lower, as in (1), then nothing new ever evolves.
    The authors think real biological organisms are closer to position (1). Indeed, study in the field of systems biology increasingly finds that biological systems contain very little junk.,,,
    http://www.evolutionnews.org/2.....95121.html

    Supplemental question Zach, since ‘random’, as it is used by Darwinists, is more or less synonymous with the word ‘miracle’, why are you an atheist instead of a Christian Theist since you believe in miracles?

    Nobel Prize-Winning Physicist Wolfgang Pauli on the Empirical Problems with Neo-Darwinism – Casey Luskin – February 27, 2012
    Excerpt: “In discussions with biologists I met large difficulties when they apply the concept of ‘natural selection’ in a rather wide field, without being able to estimate the probability of the occurrence in a empirically given time of just those events, which have been important for the biological evolution. Treating the empirical time scale of the evolution theoretically as infinity they have then an easy game, apparently to avoid the concept of purposesiveness. While they pretend to stay in this way completely ‘scientific’ and ‘rational,’ they become actually very irrational, particularly because they use the word ‘chance’, not any longer combined with estimations of a mathematically defined probability, in its application to very rare single events more or less synonymous with the old word ‘miracle.'”
    Wolfgang Pauli (pp. 27-28) –
    http://www.evolutionnews.org/2.....56771.html

    Actually on a more serious note Zach, (as if there can possibly be a more serious note than a person’s eternal salvation in Christ), since ‘unguided randomness’ forms the basis of Darwinism’s theoretical core, unguided randomness prevents Darwinism from every becoming a proper scientific theory instead of the pseudo-scientific theory that it is:

    Murray Eden, as reported in “Heresy in the Halls of Biology: Mathematicians Question Darwinism,” Scientific Research, November 1967, p. 64.
    “It is our contention that if ‘random’ is given a serious and crucial interpretation from a probabilistic point of view, the randomness postulate is highly implausible and that an adequate scientific theory of evolution must await the discovery and elucidation of new natural laws—physical, physico-chemical, and biological.”
    Murray Eden, “Inadequacies of Neo-Darwinian Evolution as a Scientific Theory,” Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution, editors Paul S. Moorhead and Martin M. Kaplan, June 1967, p. 109.
    http://www.creationscience.com.....tes32.html

  14. 14
    bornagain77 says:

    Thanks Virgil @ 10. I believe you are referring to this study:

    Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) – October 2010
    Excerpt: “Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, “This research really upends the dominant paradigm about how species evolve,” said ecology and evolutionary biology professor Anthony Long, the primary investigator.
    http://www.arn.org/blogs/index.....ruit_flies
    http://eebweb.arizona.edu/nach.....l_2010.pdf

  15. 15
    Zachriel says:

    bornagain77: With all that hand waving that you do Zach you must be staying very cool this summer.

    Actually, we answered your questions directly.

    bornagain77: 1. Since Darwinism is a non-falsifiable pseudo-science, Darwinism is consistent with anything and everything that may be found.

    This is directly contrary to your previous statement, that neodarwinism isn’t consistent with large numbers of non-beneficial mutations.

    bornagain77: 2. Darwinism does not predict ‘local optimums’. In fact supposed Bad Designs, that are supposedly not optimum, (based on the ignorance of Darwinists I might add), have been a staple of Darwinism’s theological core argument against design since day one.

    Here you conflate local optimum with global optimum. A lineage can be trapped on a local peak, while a higher peak is nearby but not reachable in a stepwise fashion. That’s why many adaptations appear to be kludges or workarounds.

  16. 16
    Eric Anderson says:

    The increasing problems with the molecular clock are interesting and stand in contrast to the party line we often hear. I seem to recall a discussion in this forum a while back regarding the molecular clock as it relates to humans and divergence from a recent common ancestor. wd400 (if I recall) was supportive of the calculations, but it seems the calculation turned out to be somewhat circular.

    In any event, it is likely that we are dealing with more than one phenomenon, which is no doubt part of the reason for the disconnect.

    1. We can measure with some reasonable accuracy the rate of mutations from generation to generation. That is simply an observational measurement and ought not to be particularly controversial.

    2. On the other hand, that mutation rate is then subjected to the following further extrapolations and assumptions, only some of which may be reasonable:

    (i) The mutation rate is assumed to be relatively constant. I would say that this is probably a reasonable assumption, absent specific reasons to think otherwise.

    (ii) It is assumed that the basic generation-to-generation random mutation changes that don’t provide any significant observable evolutionary change nevertheless, over time, accumulate into vast evolutionary changes. This is an assumption for which there is no real empirical support. It is simply an article of faith of the theory.

    (iii) It is assumed that organism A is “related” to organism B, based on genetic or morphological similarities and that, therefore, there must be some unbroken evolutionary chain linking the two. This is an assumption for which there is no observational support. It might be true, but unfortunately we cannot confirm it — the actual sequence of events leading from A to B being unfortunately buried in the detritus of time. So it remains but an assumption of the theory.

    Furthermore, this impression of “relatedness” has been compounded by poor studies and faulty thinking about what constitutes relatedness. For example, the oft-cited 98% similarity between humans and chimps (or 99% or 95% or whatever your preferred number) is based on a very simplistic and facile (and almost certainly wrong) view of what constitutes DNA “equivalence,” as well as a simplistic and facile (and almost certainly wrong) view of DNA’s role in organismal development.

    —–

    As with so many things in biology, there is a disconnect between the observational science and the historical narrative. #1 is a good, hard fact: it is real; it is observable; it is good science. In contrast, #2 is a story, a narrative “explanation” for some alleged long-past historical causal chain of events.

  17. 17
    bornagain77 says:

    Zach, I’m satisfied with the exchange thus far, and will let the unbiased reader judge for themselves who is providing solid evidence for his position and who is out in left field day-dreaming that he has any evidence whatsoever.

    Good day!

  18. 18
    Eric Anderson says:

    Zachriel @12:

    I know you are talking with BA77 and I don’t intend to get into a discussion right now, but for our readers and lurkers this jumped out at me:

    “Because most functional complexes are already at local optimums, so any change is likely to be detrimental.”

    This is nonsense. There is scarcely a biological system in existence that couldn’t be improved in some absolute sense. Wouldn’t it be better for the cheetah if she could run a bit faster, or leap a bit higher, or see a bit farther? Of course it would. And the same is true of every other organism.

    The entire edifice of Darwinian evolutionary thought that rests squarely on the idea of “slight successive changes” leading inexorably over time to biological improvement is shown to be nothing more than a confession of ignorance and an ad-hoc rationalization.

    We are constantly being informed by evolutionary proponents that nature is full of sub-par designs, poorly-cobbled-together jumbles, occasional meaningful sequences swimming in a sea of junk DNA. Yet Zachriel now tells us that most biological systems are “at local optimums,” not likely to tolerate further changes. So which is it? The story seems to change depending on the rhetorical stance needed in a particular case.

    If one looks at biological systems for what they clearly are — islands of design that take into account trade-offs of performance with functional constraints and parameters, rather than Darwin’s “plastic” organisms that can move imperceptibly from A to B to C through a series of “slight successive changes,” then the overall picture starts to make some sense.

    Or we can adopt the evolutionary “logic”: biological systems are at their local optimum, which is why we don’t actually see biological systems evolving; but biology is full of sub-optimal systems, which is what we would expect for a chaotic trial-and-error process.

    Biological systems are exquisitely formed; except when they aren’t. They are optimal; expect when they aren’t. Some are. Some aren’t.

    Yet another example of the Great Evolutionary Explanation:

    Stuff Happens.

  19. 19
    wd400 says:

    We are constantly being informed by evolutionary proponents that nature is full of sub-par designs, poorly-cobbled-together jumbles, occasional meaningful sequences swimming in a sea of junk DNA. Yet Zachriel now tells us that most biological systems are “at local optimums,” not likely to tolerate further changes. So which is it?

    Did you miss the word “local”.

  20. 20
    Virgil Cain says:

    Zachriel:

    Modern genetics has found that most mutations are random with respect to fitness,

    The debate is whether or not the mutations are happenstance events or not. “Random with respect to fitness” is irrelevant in that regard.

  21. 21
    Carpathian says:

    Eric Anderson:

    We are constantly being informed by evolutionary proponents that nature is full of sub-par designs, poorly-cobbled-together jumbles, occasional meaningful sequences swimming in a sea of junk DNA. Yet Zachriel now tells us that most biological systems are “at local optimums,” not likely to tolerate further changes. So which is it? The story seems to change depending on the rhetorical stance needed in a particular case.

    It is the systems that are “at local optimums”, not individuals.

    If predators suddenly become more efficient overnight, their prey may be at risk of extinction.

    If this happens, both prey and predator populations will suffer.

    Evolution is more concerned about populations than it is about individuals.

  22. 22
    Virgil Cain says:

    Evolution requires reproduction and populations do not reproduce. What population do is reign in the marginal, ie the mutants.

    Also unguided evolution does not produce optimal- local or otherwise.

  23. 23
    wd400 says:

    Carpathian.

    What? No. There are plenty of cases of predator-driven extinctions, after all.

  24. 24
    Carpathian says:

    Virgil Cain:

    The debate is whether or not the mutations are happenstance events or not. “Random with respect to fitness” is irrelevant in that regard.

    It is actually the point of this whole debate.

    If most mutations are “random with respect to fitness”, that is an argument for non-ID evolution.

  25. 25
    Virgil Cain says:

    Carpathian:

    If most mutations are “random with respect to fitness”, that is an argument for non-ID evolution.

    How so? Being random with respect to fitness does not mean they were unguided, ie genetic accidents. You are confused.

  26. 26
    Carpathian says:

    wd400:

    What? No. There are plenty of cases of predator-driven extinctions, after all.

    Yes and we humans are probably the worst, but in a working stable system, both prey and predators have reached a level where each can maintain stable populations regardless of any disadvantages that individual organisms may have.

    The point I was making is that you cannot “fix” bad “design” and expect that population-wise, the ecosystem will benefit.

    Flaws of individual “designs” are handled well by non-ID evolution.

  27. 27
    Virgil Cain says:

    Yes, FLAWS can be accounted for by non-ID evolution. Very good, you are starting to learn.

  28. 28
    Carpathian says:

    Virgil Cain:

    How so? Being random with respect to fitness does not mean they were unguided, ie genetic accidents. You are confused.

    I expect that any mutation that is guided by an ID designer would not be wasted.

    If the intelligent designer has a goal, he would be guiding his mutations toward it.

    A change that is not goal-directed however, is exactly what you would expect with non-ID evolution since it does not have a “target” it is working toward.

    Fitness is the “target” of the population yet non-ID evolution doesn’t have one, so this is exactly what you would expect to see.

  29. 29
    Carpathian says:

    Virgil Cain:

    Yes, FLAWS can be accounted for by non-ID evolution. Very good, you are starting to learn.

    Exactly.

    The flaws we see in the “design” of organisms points to non-ID evolution as being the cause.

    Looks like we’re both learning.

  30. 30
    Virgil Cain says:

    Carpathisn:

    I expect that any mutation that is guided by an ID designer would not be wasted.

    ID doesn’t require that any mutations be guided by a designer. Spellcheck doesn’t require a programmer be there to change the incorrect spelling.

    If the intelligent designer has a goal, he would be guiding his mutations toward it.

    You are confused and ignorant of ID.

    A change that is not goal-directed however, is exactly what you would expect with non-ID evolution since it does not have a “target” it is working toward.

    Which is exactly why it cannot produce the types of changes universal common descent requires.

  31. 31
    Virgil Cain says:

    Carpathian:

    The flaws we see in the “design” of organisms points to non-ID evolution as being the cause.

    That is what we have been saying for years. You cannot expect flaws to add up to something useful.

  32. 32
    Mung says:

    Carpathian: Evolution is more concerned about populations than it is about individuals.

    I certainly never felt any concern of evolution about me, but I also don’t see why evolution would be concerned about humans in general either.

  33. 33
    Carpathian says:

    Virgil Cain:

    If the intelligent designer has a goal, he would be guiding his mutations toward it.

    You are confused and ignorant of ID.

    1) How can something intelligent not have a goal? That is the whole point of ID, that there is a “target” which needs to be “designed” since a non-ID solution is improbable.

    2) If the intelligent designer does not have a goal, why do his designs work?

    3) If a goal isn’t required, how can non-ID be improbable?

    If there is no “target”, there is no solution that is “improbable”.

    Behe suggests IC is goal-oriented since the designs he mentions are irreducible, i.e. every part must be there.

    This points to a goal.

  34. 34
    wd400 says:

    I’d give up Carpathian. This is one of Joe/Virgil’s weird and unshakeable beliefs. The fact it leaves his version of ID completely untestable doesn’t seem to worry him.

  35. 35
    Virgil Cain says:

    Carpathian:

    1) How can something intelligent not have a goal?

    That doesn’t mean a designer is guiding the mutations. Dr Spetner has posited a “non-random evolutionary hypothesis” with “built-in responses to environmental cues” as the main mechanism. BUILT-IN.

    That is the whole point of ID, that there is a “target” which needs to be “designed” since a non-ID solution is improbable.

    Unguided evolution is impotent. That is why something else is required to explain the evidence and the evidence fits the design criteria.

    ID doesn’t require that any mutations be guided by a designer. Spell check doesn’t require a programmer be there to change the incorrect spelling.

    Did you read that part or do you not understand it?

  36. 36
    Virgil Cain says:

    wd400:

    The fact it leaves his version of ID completely untestable doesn’t seem to worry him.

    Unguided evolution is completely untestable and that doesn’t seem to worry evolutionists. We can and have modeled intelligently designed evolution with evolutionary and genetic algorithms. We cannot model unguided evolution producing something like a bacterial flagellum.

  37. 37
    Carpathian says:

    wd400:

    I’d give up Carpathian. This is one of Joe/Virgil’s weird and unshakeable beliefs. The fact it leaves his version of ID completely untestable doesn’t seem to worry him.

    He does sound like Joe!

    What he has done here is retracted from full ID to something closer to Darwinism.

  38. 38
    Virgil Cain says:

    Carpathian:

    What he has done here is retracted from full ID to something closer to Darwinism.

    How do you figure? “Not By Chance” was published in 1997- that means your misunderstanding is inexcusable.

  39. 39
    Carpathian says:

    Virgil Cain,

    ID is supposed to solve the problem of “finding” the “target”.

    This implies ID must know what the target actually is.

    Without guidance from an intelligent designer, the “built-in” guidance system cannot “identify” the “target”.

    The problem with your version of ID is it leaves out the intelligence that “specifies” the “target”.

  40. 40
    Virgil Cain says:

    Carpathian, Just admit that you don’t know anything about ID and you are making it up as you go.

    Without guidance from an intelligent designer, the “built-in” guidance system cannot “identify” the “target”.

    And yet evolutionary and genetic algorithms find the solution without any guidance from the designer other than the program.

    The problem with your version of ID is it leaves out the intelligence that “specifies” the “target”.

    The intelligence is in the program- see spell check.

  41. 41
    Carpathian says:

    Virgil Cain:

    The problem with your version of ID is it leaves out the intelligence that “specifies” the “target”.

    The intelligence is in the program- see spell check.

    Just where in the cell is this “specifier of targets” found?

    How does DNA or any other biological construction look into the future and intelligently determine a “specified target”?

  42. 42
    Mung says:

    Carpathian: ID is supposed to solve the problem of “finding” the “target”.

    Evolution is supposed to solve the problem of “finding” the “target”.

    Carpathian: This implies ID must know what the target actually is.

    This implies that your “weasel” program must know what the target is.

    Carpathian: Without guidance from an intelligent designer, the “built-in” guidance system cannot “identify” the “target”.

    Yes, your “weasel” program works not because it simulates “evolution” but because it was intelligently designed. We tried to tell you this. repeatedly.

  43. 43
    bornagain77 says:

    I have another question for neo-Darwinists, (i.e. Zach, wd400, carp, etc..), about random mutations as they pertain to neo-Darwinism.
    How can random mutations to DNA possibly be the creative fodder for neo-Darwinian evolution when an organism’s body plan is not even reducible to random mutations to DNA in the first place as is presupposed in neo-Darwinism?

    Response to John Wise – October 2010
    Excerpt: A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.
    http://www.evolutionnews.org/2.....38811.html

    ‘No matter what we do to a fruit fly embryo there are only three possible outcomes, a normal fruit fly, a defective fruit fly, or a dead fruit fly. What we never see is primary speciation much less macro-evolution’ –
    Jonathan Wells
    Darwin’s Theory – Fruit Flies and Morphology – video
    http://www.youtube.com/watch?v=hZJTIwRY0bs

    Peer-Reviewed Paper: Development Needs Ontogenetic Information that Cannot Arise from Neo-Darwinian Mechanisms – Casey Luskin – June 2, 2014
    Excerpt: ,,,”the vast majority of proteins in eukaryotes are not completely specified by DNA sequences.”,,,
    Jonathan Wells
    http://www.evolutionnews.org/2.....86201.html

    I went to Wells’s paper and found on page 11:

    Membrane Patterns Carry Ontogenetic Information That Is Specified Independently of DNA – 2014 – Jonathan Wells
    Excerpt Page 11: Most proteins are not completely specified by DNA sequences:
    The central dogma (which here includes Crick’s sequence hypothesis) claims that (1) DNA specifies RNA and (2) RNA specifies protein. Yet this claim fails at both steps, because most RNAs are not uniquely specified by DNA sequences, and many proteins are not uniquely specified by RNAs—either in their amino acid sequences or in their final folded forms. After transcription, RNAs from many eukaryotic genes undergo alternative splicing. Recent studies estimate that transcripts from approximately 95% of multi-exon human genes are spliced in more than one way [289?291]. By intervening between transcription and translation, alternative splicing generates RNAs with sequences that differ from DNA sequences [292]. The differences are functionally significant.,,,
    Page 12
    In addition to alternative splicing, many metazoan transcripts undergo RNA editing, which can (a) modify cytidine to uridine; (b) modify adenosine to inosine; or (c) insert additional nucleotides. Several recent analyses have demonstrated extensive RNA editing in the human transcriptome [303?305]. The editing of an mRNA often alters the amino acid sequence of the encoded protein so that it differs from the sequence predicted by the DNA [306,307].
    References:
    289. Wang ET, Sandberg R, Luo S, Khrebtukova I, Zhang L, et al. (2008) Alternative isoform regulation in human tissue transcriptomes. Nature 456:470-476. doi: 10.1038/nature07509
    290. Pan Q, Shai O, Lee LJ, Frey BJ, Blencowe BJ (2008) Deep surveying of alternative splicing complexity in the human transcriptome by high-throughput sequencing. Nat Genet 40:1413-1415. doi: 10.1038/ng.259
    291. Barash Y, Calarco JA, Gao W, Pan Q, Wang X, et al. (2010) Deciphering the splicing code. Nature 465:53-59. doi: 10.1038/nature09000
    292. Kornblihtt AR, Schor IE, Alló M, Dujardin G, Petrillo E, et al. (2013) Alternative splicing: A pivotal step between eukaryotic transcription and translation. Nat Rev Mol Cell Biol 14:153-165. doi: 10.1038/nrm3525
    303. Peng Z, Cheng Y, Tan BC, Kang L, Tian Z, et al. (2012) Comprehensive analysis of RNA-Seq data reveals extensive RNA editing in a human transcriptome. Nat Biotechnol 30:253-260. doi: 10.1038/nbt.2122
    304. Bahn JH, Lee JH, Li G, Greer C, Peng G, et al. (2012) Accurate identification of A-to-I RNA editing in human by transcriptome sequencing. Genome Res 22:142-150. doi: 10.1101/gr.124107.111
    305. Sakurai M, Ueda H, Yano T, Okada S, Terajima H (2014) A biochemical landscape of A-to-I RNA editing in the human brain transcriptome. Genome Res (January 9, 2014). doi: 10.1101/gr.162537.113
    306. Brennicke A, Marchfelder A, Binder S (1999) RNA editing. FEMS Microbiol Rev 23:297-316. doi: 10.1111/j.1574-6976.1999.tb00401.x
    307. Eisenberg E, Li JB, Levanon EY (2010) Sequence based identification of RNA editing sites. RNA Biol 7:248-252. doi: 10.4161/rna.7.2.11565
    http://bio-complexity.org/ojs/.....O-C.2014.2

    In fact, completely contrary to neo-Darwinian thought, it’s the organism controlling the DNA, not the DNA controlling the organism:

    Ask an Embryologist: Genomic Mosaicism – Jonathan Wells – February 23, 2015
    Excerpt: humans have a “few thousand” different cell types. Here is my simple question: Does the DNA sequence in one cell type differ from the sequence in another cell type in the same person?,,,
    The simple answer is: We now know that there is considerable variation in DNA sequences among tissues, and even among cells in the same tissue. It’s called genomic mosaicism.
    In the early days of developmental genetics, some people thought that parts of the embryo became different from each other because they acquired different pieces of the DNA from the fertilized egg. That theory was abandoned,,,
    ,,,(then) “genomic equivalence” — the idea that all the cells of an organism (with a few exceptions, such as cells of the immune system) contain the same DNA — became the accepted view.
    I taught genomic equivalence for many years. A few years ago, however, everything changed. With the development of more sophisticated techniques and the sampling of more tissues and cells, it became clear that genetic mosaicism is common.
    I now know as an embryologist,,,Tissues and cells, as they differentiate, modify their DNA to suit their needs. It’s the organism controlling the DNA, not the DNA controlling the organism.
    http://www.evolutionnews.org/2.....93851.html

    Dr. Meyer puts the insurmountable ‘body plan’ problem for neo-Darwinists as such:

    ‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’
    Stephen Meyer – (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate – 2009)
    – Functional Proteins and Information for Body Plans – video
    https://vimeo.com/91322260

    Dr. Meyer’s preceding comment elucidates a huge question that is never honestly addressed by our resident neo-Darwinists.
    Namely, even if neo-Darwinian evolution were to somehow, miraculously, stumble onto a functional protein, how in blue blazes does the neo-Darwinism figure out what to do with the new protein?
    Stephen L. Talbott puts the problem as such:

    HOW BIOLOGISTS LOST SIGHT OF THE MEANING OF LIFE — AND ARE NOW STARING IT IN THE FACE – Stephen L. Talbott – May 2012
    Excerpt: “If you think air traffic controllers have a tough job guiding planes into major airports or across a crowded continental airspace, consider the challenge facing a human cell trying to position its proteins”. A given cell, he notes, may make more than 10,000 different proteins, and typically contains more than a billion protein molecules at any one time. “Somehow a cell must get all its proteins to their correct destinations — and equally important, keep these molecules out of the wrong places”. And further: “It’s almost as if every mRNA [an intermediate between a gene and a corresponding protein] coming out of the nucleus knows where it’s going” (Travis 2011),,,
    Further, the billion protein molecules in a cell are virtually all capable of interacting with each other to one degree or another; they are subject to getting misfolded or “all balled up with one another”; they are critically modified through the attachment or detachment of molecular subunits, often in rapid order and with immediate implications for changing function; they can wind up inside large-capacity “transport vehicles” headed in any number of directions; they can be sidetracked by diverse processes of degradation and recycling… and so on without end. Yet the coherence of the whole is maintained.
    The question is indeed, then, “How does the organism meaningfully dispose of all its molecules, getting them to the right places and into the right interactions?”
    The same sort of question can be asked of cells, for example in the growing embryo, where literal streams of cells are flowing to their appointed places, differentiating themselves into different types as they go, and adjusting themselves to all sorts of unpredictable perturbations — even to the degree of responding appropriately when a lab technician excises a clump of them from one location in a young embryo and puts them in another, where they may proceed to adapt themselves in an entirely different and proper way to the new environment. It is hard to quibble with the immediate impression that form (which is more idea-like than thing-like) is primary, and the material particulars subsidiary.
    Two systems biologists, one from the Max Delbrück Center for Molecular Medicine in Germany and one from Harvard Medical School, frame one part of the problem this way:
    “The human body is formed by trillions of individual cells. These cells work together with remarkable precision, first forming an adult organism out of a single fertilized egg, and then keeping the organism alive and functional for decades. To achieve this precision, one would assume that each individual cell reacts in a reliable, reproducible way to a given input, faithfully executing the required task. However, a growing number of studies investigating cellular processes on the level of single cells revealed large heterogeneity even among genetically identical cells of the same cell type. (Loewer and Lahav 2011)”,,,
    And then we hear that all this meaningful activity is, somehow, meaningless or a product of meaninglessness. This, I believe, is the real issue troubling the majority of the American populace when they are asked about their belief in evolution. They see one thing and then are told, more or less directly, that they are really seeing its denial. Yet no one has ever explained to them how you get meaning from meaninglessness — a difficult enough task once you realize that we cannot articulate any knowledge of the world at all except in the language of meaning.,,,
    http://www.netfuture.org/2012/May1012_184.html#2

    Of supplemental note, where chimps and humans differ by ‘orders of magnitude’ is in the regulatory networks

    “Where (chimps and humans) really differ, and they differ by orders of magnitude, is in the genomic architecture outside the protein coding regions. They are vastly, vastly, different.,, The structural, the organization, the regulatory sequences, the hierarchy for how things are organized and used are vastly different between a chimpanzee and a human being in their genomes.”
    Raymond Bohlin (per Richard Sternberg)

    Richard Sternberg PhD – podcast – On Human Origins: Is Our Genome Full of Junk DNA? Part 2
    http://www.discovery.org/multi.....-dna-pt-2/

    Yet random mutations to regulatory networks are ‘always catastrophically bad’

    A Listener’s Guide to the Meyer-Marshall Debate: Focus on the Origin of Information Question -Casey Luskin – December 4, 2013
    Excerpt: “There is always an observable consequence if a dGRN (developmental gene regulatory network) subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.” –
    Eric Davidson
    http://www.evolutionnews.org/2.....79811.html

    Thus, where neo-Darwinists most need plasticity in the genome to be viable as a theory, (i.e. developmental Gene Regulatory Networks), is the place where mutations are found to be ‘always catastrophically bad’. Yet, it is exactly in this area of the genome (i.e. regulatory networks) where substantial, ‘orders of magnitude’, differences are found between even supposedly closely related species (even chimps and humans).
    Needless to say, this is the exact opposite finding for what Darwinism would have predicted for what should have been found in the genome.
    If neo-Darwinism were a normal science, instead of being the creation myth for atheists, this finding, by all rights, should have falsified neo-Darwinism by itself.

  44. 44
    Virgil Cain says:

    Carpathian:

    Just where in the cell is this “specifier of targets” found?

    Everywhere. Try building a living cell without the proper software.

    How does DNA or any other biological construction look into the future and intelligently determine a “specified target”?

    Why do you ask such leading questions that tend to expose your strawman version? And why do you refuse to respond to my points that explain my claim?

  45. 45
    Virgil Cain says:

    “Not By Chance” was published in 1997, meaning guided mutations is not my version. And it only makes sense that if life was intelligently designed that the bulk of the change would be part and parcel of that intelligent design, ie guided.

  46. 46
    Zachriel says:

    Eric Anderson: Wouldn’t it be better for the cheetah if she could run a bit faster, or leap a bit higher, or see a bit farther?

    There’s always a tradeoff involved. The cheetah is a powerful predator, but if she misses very many opportunities, she won’t have enough energy to breed or care for offspring.

    Eric Anderson: Yet Zachriel now tells us that most biological systems are “at local optimums,” not likely to tolerate further changes. So which is it?

    Being on a local peak means having to descend to reach a higher peak. Stabilizing selection is a very common type of selection.

  47. 47
    Mung says:

    So how do we test the claim that some species is on a local optima or that some species is or is not under stabilizing selection?

  48. 48
    wd400 says:

    Directly. You mutate them or collect natural mutants and measure their fitness.

    You can also use population genetics to detect historical and recent stabilizing selection, which is near universal in protein coding genes.

  49. 49
    bornagain77 says:

    “There’s always a tradeoff involved.”

    The ‘tradeoffs’ are actually design constraints that expose, once again, Darwinian explanations as fantasy

    “This is the issue I have with neo-Darwinists: They teach that what is generating novelty is the accumulation of random mutations in DNA, in a direction set by natural selection. If you want bigger eggs, you keep selecting the hens that are laying the biggest eggs, and you get bigger and bigger eggs. But you also get hens with defective feathers and wobbly legs. Natural selection eliminates and maybe maintains, but it doesn’t create….
    (Quoted in “Discover Interview: Lynn Margulis Says She’s Not Controversial, She’s Right,” Discover Magazine, p. 68 (April, 2011).)

    GMO Bulls Now A Reality – January 11, 2014
    Excerpt: “Due to genetic selection and experiments, the Belgian Blue is a humongous species of Bull, packed with muscles and meat.
    …There is a gene that regulates the growth of muscles in cattle, These cows have been selectively bred from animals that contain a copy of this gene that doesn’t work, as a result their muscles grow far larger than normal [They have a deletion mutation that prevents control of muscular growth = loss of genetic material].
    ..Their uninhibited muscle growth presents a lot of health hazards, calves can develop enlarged tongues and stiff legs which make it difficult for them to eat and move, leading to an early and painful death.”
    http://naturalhealthwarriors.c.....a-reality/

    K´necting The Dots: Modeling Functional Integration In Biological Systems – June 11, 2010
    Excerpt: “If an engineer modifies the length of the piston rods in an internal combustion engine, but does not modify the crankshaft accordingly, the engine won’t start. Similarly, processes of development are so tightly integrated temporally and spatially that one change early in development will require a host of other coordinated changes in separate but functionally interrelated developmental processes downstream” (1)
    http://www.uncommondescent.com.....l-systems/

    THE PROBLEM OF CONSTRAINTS ON VARIATION, FROM DARWIN TO THE PRESENT – IGOR POPOV – 2009
    Excerpt: There are limitations to variability. “The real number of variations is lesser than expected one. There are no blue-eyed Drosophila, no viviparous birds or turtles, no hexapod mammals, etc. Such observations provoke non-Darwinian evolutionary concepts. Darwin tried rather unsuccessfully to solve the problem of the contradictions between his model of random variability and the existence of constraints. He tried to hide this complication citing abundant facts on other phenomena. The authors of the modern versions of Darwinism followed this strategy, allowing the question to persist. …However, he was forced to admit some cases where creating anything humans may wish for was impossible. For example, when the English farmers decided to get cows with thick hams, they soon abandoned this attempt since they perished too frequently during delivery. Evidently such cases provoked an idea on the limitations to variability… The problem of the constraints on variation was not solved neither within the framework of the proper Darwin’s theory, nor within the framework of modern Darwinism.”
    http://www.ludusvitalis.org/te....._popov.pdf

  50. 50
    bornagain77 says:

    It is impossible for Darwinian processes to reach ‘optimum’, whether it be local optimum, global optimum, or whatever optimum:

    Study demonstrates evolutionary ‘fitness’ not the most important determinant of success – February 7, 2014 – with illustration
    Excerpt: An illustration of the possible mutations available to an RNA molecule. The blue lines represent mutations that will not change its function (phenotype), the grey are mutations to an alternative phenotype with slightly higher fitness and the red are the ‘fittest’ mutations. As there are so few possible mutations resulting in the fittest phenotype in red, the odds of this mutation are a mere 0.15%. The odds for the slightly fitter mutation in grey are 6.7% and so this is far more likely to fix, and thus to be found and survive, even though it is much less fit than the red phenotype.,,,
    By modelling populations over long timescales, the study showed that the ‘fitness’ of their traits was not the most important determinant of success. Instead, the most genetically available mutations dominated the changes in traits. The researchers found that the ‘fittest’ simply did not have time to be found, or to fix in the population over evolutionary timescales.
    http://phys.org/news/2014-02-e.....ccess.html

    This following headline sums the preceding finding up very nicely:

    Fittest Can’t Survive If They Never Arrive – February 7, 2014
    http://crev.info/2014/02/fitte.....er-arrive/

    William Bialek: More Perfect Than We Imagined – March 23, 2013
    Excerpt: photoreceptor cells that carpet the retinal tissue of the eye and respond to light, are not just good or great or phabulous at their job. They are not merely exceptionally impressive by the standards of biology, with whatever slop and wiggle room the animate category implies. Photoreceptors operate at the outermost boundary allowed by the laws of physics, which means they are as good as they can be, period. Each one is designed to detect and respond to single photons of light — the smallest possible packages in which light comes wrapped.
    “Light is quantized, and you can’t count half a photon,” said William Bialek, a professor of physics and integrative genomics at Princeton University. “This is as far as it goes.” …
    Scientists have identified and mathematically anatomized an array of cases where optimization has left its fastidious mark, among them;,, the precision response in a fruit fly embryo to contouring molecules that help distinguish tail from head;,,, In each instance, biophysicists have calculated, the system couldn’t get faster, more sensitive or more efficient without first relocating to an alternate universe with alternate physical constants.
    http://darwins-god.blogspot.co.....an-we.html

  51. 51
    scottH says:

    BA77 you are a machine! I learn a lot from your links. Keep it up!

  52. 52
    mike1962 says:

    BA77 @43,49,50

    You’re kicking some serious butt.

  53. 53
    ppolish says:

    Me too, ScottH re BA77. He has helped me “unlearn” a bunch too (I was raised as a Darwinist). The Darwin Delusion;)

  54. 54
    Virgil Cain says:

    There’s always a tradeoff involved.

    Just another reason why variation is limited and universal common descent out of reach.

  55. 55
    bornagain77 says:

    Well thanks guys. It sure is a change from angrily being called an IDiot.

    Verse and Music:

    Colossians 2:2-4
    ,, unto all riches of the full assurance of understanding, that they may know the mystery of God, even Christ,
    in whom are all the treasures of wisdom and knowledge hidden.
    This I say, that no one may delude you with persuasiveness of speech.

    Jamie Grace – Beautiful Day (Official Lyric Video)
    https://www.youtube.com/watch?v=uPy0ctqMwE0

  56. 56
    Silver Asiatic says:

    Stabilizing selection, LOL
    Sometimes selection wants to stabilize. Sometimes it wants to be directional. Sometimes it wants to be disruptive. Stuff happens. It’s all about fitness.

    Fitness measurements, LOL

    After 35 years and 600 generations, accelerated by artificial selection:

    We conclude that, at least for life history characters such as development time, unconditionally advantageous alleles rarely arise, are associated with small net fitness gains or cannot fix because selection coefficients change over time.

    Burke, Dunham et al, “Genome-wide analysis of a long-term evolution experiment with Drosophila,” Nature 467, 587–590 (30 September 2010); doi:10.1038/nature09352.

    Selection coefficients change over time?
    No problem – we’ll just assume that fitness criteria remains constant and when an organism reaches a ‘local optimum’ then stabilizing selection kicks in. The organism needs to develop legs, wings, eyes, digestive and reproductive systems first in order to reach ‘local optimum’, of course, but once it got there, all it needs is “stabilizing”.

    Need to develop some echo-location functions? Moving into the water and need fins, a change of diet and a blow-hole? Disruptive selection is what you’re looking for — and it will be there, as long as you’re not in a local optimum. In that case, you’re out of luck.

    Stabilizing selection (not the same thing as negative selection[1][2]) is a type of natural selection in which genetic diversity decreases and the population mean stabilizes on a particular trait value. This is thought to be the most common mechanism of action for natural selection because most traits do not appear to change drastically over time. [3] Stabilizing selection commonly uses negative selection (a.k.a. purifying selection) to select against extreme values of the character …
    Because most traits change little over time, stabilizing selection is thought to be the most common type of selection in most populations. [6] However, a meta-analysis of studies that measured selection in the wild failed to find an overall trend for stabilizing selection. [7] The reason can be that methods for detecting stabilizing selection are complex. They can involve studying the changes that causes natural selection in the mean and variance of the trait, or measuring fitness for a range of different phenotypes under natural conditions and examining the relationship between these fitness measurements and the trait value, but analysis and interpretation of the results is not straightforward.

    It’s the most common method of selection we can’t find a trend in the wild? Analysis and interpretation of the statistics is not straightforward?

    Come on – run a few correlations.

  57. 57
    Axel says:

    Yes. It’s great to see you getting some of the plaudits you’ve so richly deserved, BA77.

    A new twist on God doesn’t make mistakes in his handiwork! You’re a divine work of art in yourself, over and above your ‘common’ humanity. A veritable light unto the scientific world, and to the rest of humanity

  58. 58
    Dionisio says:

    Axel, scottH, mike1962, ppolish,
    agree with your comments about the impacting work BA77 does here:
    Providing very interesting information in almost all the discussion threads. I don’t know how he does that. Really impressive.

    BTW, you all may want to look at this reference to a very recent paper (note the highlighted text):

    http://www.uncommondescent.com.....ent-569129

  59. 59
    Carpathian says:

    Mung:

    Carpathian: ID is supposed to solve the problem of “finding” the “target”.

    Mung: Evolution is supposed to solve the problem of “finding” the “target”.

    It is ID that claims the existence of a “target”, not evolution.

    Ask kairosfocus what the S in CSI stands for.

    Evolution does not have a “target” to “find” since anything that survives to reproduce has implicitly been “accepted” by the environment.

    Carpathian: This implies ID must know what the target actually is.
    Mung: This implies that your “weasel” program must know what the target is.

    Carpathian: Without guidance from an intelligent designer, the “built-in” guidance system cannot “identify” the “target”.

    Mung: Yes, your “weasel” program works not because it simulates “evolution” but because it was intelligently designed. We tried to tell you this. repeatedly.

    A “weasel” program serves the same purpose as an oscilloscope.

    They are both used to investigate reality but are themselves not the devices under test.

    You don’t seem to understand the difference between the map and the territory.

    Ask kairosfocus why a meter shouldn’t be considered a part of the battery it is measuring.

    You could also ask a tailor why a measuring tape is not part of the suit he is making.

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